Artículos de revistas
Mice lacking neuronal calcium sensor-1 show social and cognitive deficits
Registro en:
Behavioural Brain Research, Volume 381, 2 March 2020, 112420
0166-4328
10.1016/j.bbr.2019.112420
Autor
Ng, Enoch
Georgiou, John
Ávila, Ariel
Trought, Kathleen
Mun, Ho-Suk
Hodgson, Meggie
Servinis, Panayiotis
Roder, John C.
Collingridge, Graham L.
Wong, Albert H.C
Resumen
Artículo de publicación ISI Neuronal calcium sensor-1 or Frequenin is a calcium sensor widely expressed in the nervous system, with roles in neurotransmission, neurite outgrowth, synaptic plasticity, learning, and motivated behaviours. Neuronal calcium sensor-1 has been implicated in neuropsychiatric disorders including autism spectrum disorder, schizophrenia, and bipolar disorder. However, the role of neuronal calcium sensor-1 in behavioural phenotypes and brain changes relevant to autism spectrum disorder have not been evaluated. We show that neuronal calcium sensor-1 deletion in the mouse leads to a mild deficit in social approach and impaired displaced object recognition without affecting social interactions, behavioural flexibility, spatial reference memory, anxiety-like behaviour, or sensorimotor gating. Morphologically, neuronal calcium sensor-1 deletion leads to increased dendritic arbour complexity in the frontal cortex. At the level of hippocampal synaptic plasticity, neuronal calcium sensor-1 deletion leads to a reduction in long-term potentiation in the dentate gyrus, but not area Cornu Ammonis 1. Metabotropic glutamate receptor-induced long-term depression was unaffected in both dentate and Cornu Ammonis 1. These studies identify roles for neuronal calcium sensor-1 in specific subregions of the brain including a phenotype relevant to neuropsychiatric disorders.